Differential expression of genes involved in the calcium homeostasis in masticatory muscles of mdx mice

Duchenne muscular dystrophy (dmd) and its murine model,mdx,are characterized by ca2+ induced muscle damage and muscle weakness followed by distorted dentofacial morphology. in both,dmd patients and in mdx mice,could be proven so far that only the extraocular muscles (eom) are not affected by muscular dystrophy. the eoms are protected against calcium overload by enhanced expression of genes involved in the ca2+ homeostasis. we could recently demonstrate that masticatory muscles of mdx mice are differentially affected by muscle dystrophy. the dystrophic masseter and temporalis shows muscle histology comparable to all other skeletal muscles in this animal model,whereas dystrophic tongue muscles seem to develop a milder phenotype. due to this fact it is to hypothesize that an altered ca2+ homeostasis seems to underlie the mdx masticatory muscle pathology. aim of this study was to examine the mrna and protein levels of the sarcoplasmic reticulum ca2+atpases serca1 and serca2,the plasma membrane ca2+atpases atp2b1 and atp2b4,the sodium/calcium exchanger ncx1,the ryanodine receptor 1,parvalbumin,sarcolipin,phospholamban and the l-type ca2+ channel alpha-1 subunit (cacna1s) in musculus masseter,temporalis,and tongue of 100 day old control and mdx mice. in mdx masseter muscle significant increased mrna levels of ncx1 and cacna1s were found compared to control mice. in contrast,the mrna amount of ryr1 was significant reduced in mdx temporalis muscle,whereas atp2b4 was significant increased. in mdx tongue a down-regulation of the atp2b1,sarcolipin and parvalbumin mrna expression was found,whereas the phospholamban mrna level was significantly increased compared to controls. these data were verified by western blot analyses. our findings revealed that mdx masticatory muscles showed an unequally altered expression of genes involved in the ca2+ homeostasis that can support the differences in masticatory muscles response to dystrophin deficiency.